The diagnosis of HP requires appropriate suspicion to recognize the clinical syndrome and potential antigen source. Patients may present with acute, subacute, and/or chronic symptoms, depending on the intensity and duration of antigen exposure, but disease will not develop in all exposed workers. High-resolution CT scanning is particularly useful in suggesting HP; it helps to differentiate patients with airways disease, such as occupational asthma, that may also cause work-related symptoms. Acute HP manifests following heavy exposure with fever, dyspnea, and hypoxemia; chest radiographs show airspace opacification. Subacute HP presents over weeks to months with high-resolution chest CT scan findings of centrilobular nodules and ground-glass opacification, often combined with a mosaic attenuation pattern reflecting small airways involvement. Chronic HP may closely mimic idiopathic pulmonary fibrosis clinically, with the insidious onset of dyspnea, and radiographically, with fibrotic changes tending to involve the midlung zones. There is no pathognomonic histology examination or serologic test for diagnosing HP; thus, the diagnosis depends on a combination of clinical, radiographic, and pathologic findings. MWF-related HP is often reported in the context of an epidemic, and the finding of multiple affected workers from the same job site should increase clinical suspicion. However, if a formal investigation has not occurred (as in the case reported here), patients may present to different physicians at different times, and the nature and source of the disorder may not be appreciated. Pulmonary function testing typically reveals a restrictive pattern with decreased diffusion, but concomitant airflow obstruction may be seen, especially in the presence of preexisting obstructive lung disease (as in the present case). Transbronchial lung biopsy has a high yield in HP, with supportive findings including mononuclear interstitial pneumonitis, poorly formed granulomas, and bronchiolitis obliterans with organizing pneumonia. Although frequently ordered, commercially available serum antigen panels are diagnostically insensitive (eg, they test for only a limited number of antigens) and nonspecific (eg, precipitins do not distinguish exposure from disease), and thus have limited applicability in most individual patient situations. Other evidence supporting a diagnosis of HP includes a lymphocytic alveolitis found using BAL, a low diffusing capacity of the lung for carbon monoxide, auscultatory rales, and improvement with antigen avoidance.